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1 ics into aberrant cells that overexpress the LDL receptor.
2 ultimately disrupt the interaction with the LDL receptor.
3 SK9 modulates atherosclerosis mainly via the LDL receptor.
4 e resident proteins and an ER-trapped mutant LDL receptor.
5 its role in promoting the degradation of the LDL receptor.
6 cretion is to some extent independent of the LDL receptor.
7 ic expression of SREBP-2 and its target, the LDL receptor.
8 red for clathrin-mediated endocytosis of the LDL receptor.
9 of apoE3-NT to interact with heparin and the LDL receptor.
10 erol levels by regulating the degradation of LDL receptors.
11 large VLDL, which are removed from plasma by LDL receptors.
12 ) receptor family, suggesting involvement of LDL receptors.
13 ch particles compared with mice lacking only LDL receptors.
14 teins by the liver and work independently of LDL receptors.
15 degradation of the low-density lipoprotein (LDL) receptor.
16 otein that degrades low-density lipoprotein (LDL) receptors.
17 elets via its receptor, lectin-like oxidized LDL receptor-1 (LOX-1), and alphabeta amyloid peptide, w
20 ing factor receptor and lectin-like oxidized LDL receptor-1 to attenuate Akt activation and trigger g
22 s that result in loss of function within the LDL receptor, a major determinant of inherited hyperlipi
23 hypercholesterolemia patients with defective LDL receptor activity but no reduction in those who were
24 SiRNA-depletion of Dab2 profoundly reduced LDL-receptor activity in ARH fibroblasts as a result of
27 ting furin-cleaved PCSK9 is able to regulate LDL receptor and serum cholesterol levels, although some
28 s should be the most effective in preserving LDL receptors and in lowering plasma LDL cholesterol.
30 DL) receptors, increasing the degradation of LDL receptors and reducing the rate at which LDL cholest
31 ulating the hepatic low-density lipoprotein (LDL) receptors and increasing the clearance of LDL-chole
32 binding to hepatic low-density lipoprotein (LDL) receptors and promoting their lysosomal degradation
34 pe 9) is a negative regulator of the hepatic LDL receptor, and clinical studies with PCSK9-inhibiting
35 one, with or without a genetic defect in the LDL receptor, and in subjects intolerant to statins, the
37 es involved in cholesterol biosynthesis, the LDL receptor, and PCSK9; a secreted protein that degrade
38 ced vitamin D deficiency in two backgrounds (LDL receptor- and ApoE-null mice) that resemble humans w
40 rited disorder caused by mutations either in LDL receptor, apolipoprotein B (APOB), or proprotein con
41 amilial hypercholesterolaemia-causing genes, LDL receptor, apolipoprotein B and PCSK9, the most likel
42 tics and endocytosis of LDL particles by the LDL receptor are common in the general population and in
43 antibodies that inhibit its function on the LDL receptor are evaluated in phase III clinical trials.
44 and cells have identified increased hepatic LDL receptors as the basis for LDL lowering by PCSK9 inh
45 e start with a brief introduction to LDL and LDL receptor, as well as the advantages of using rLDL pa
46 In contrast, blocking LDL receptor with RAP (LDL receptor-associated protein) stopped the internaliza
47 ase PCSK9 binds the low-density lipoprotein (LDL) receptor at the surface of hepatocytes, thereby pre
48 ese results are consistent with increases in LDL receptors available to clear IDL and LDL from blood
49 (AT2 +/y) and deficient (AT2 -/y) mice in an LDL receptor -/- background were fed a saturated-fat enr
52 ies showed that MG(min)-LDL was bound by the LDL receptor but not by the scavenger receptor and had i
53 ycle, 4) LDL-induced aneuploidy requires the LDL receptor, but not Ass, showing that LDL works differ
54 esearch on a novel regulatory pathway of the LDL receptor by PCSK9, a new class of such drugs with a
56 protein (LDL) receptor family member, termed LDL receptor class A domain containing 3 (LRAD3), which
58 s via DC-ASGPR, but not lectin-like oxidized-LDL receptor, Dectin-1, or DC-specific ICAM-3-grabbing n
59 d mice developed hyperlipidemia due to a non-LDL receptor defect in clearance of circulating apoB-con
60 ean+/-SD LDL cholesterol reductions in the 6 LDL receptor-defective patients were 19.3+/-16% and 26.3
61 ifferent populations including patients with LDL receptor defects (heterozygous familial hypercholest
63 protective role in early lesion formation in LDL receptor deficient mice, and Crry-Ig and soluble C1
69 ABCG1 in T cells impacts atherosclerosis in LDL receptor-deficient (LDLR-deficient) mice, a model of
70 afb-deficient fetal liver cells in recipient LDL receptor-deficient hyperlipidemic mice revealed acce
71 tivity and activation of coagulation in both LDL receptor-deficient mice and African green monkeys.
73 nistration of Slit2 to atherosclerosis-prone LDL receptor-deficient mice inhibited monocyte recruitme
79 n these transgenic mice were crossed with an LDL receptor-deficient mouse model and were fed a high-f
86 ithin:cholesterol acyltransferase (LCAT) and LDL receptor double knock-out mice (Ldlr(-/-)xLcat(-/-)
87 down-regulates the low-density lipoprotein (LDL) receptor, elevating LDL cholesterol and acceleratin
88 ions that work primarily via upregulation of LDL receptor expression (ie, diet, bile acid sequestrant
89 tatin therapies that act via upregulation of LDL receptor expression to reduce LDL-C were associated
92 e structures of LDL and its complex with the LDL receptor extracellular domain (LDL.LDLr) at extracel
93 omplement-type ligand binding repeats in the LDL receptor family are thought to mediate the interacti
95 general antagonist for binding of ligands to LDL receptor family members, inhibited APC-induced phosp
97 e known to be critical for ligand binding to LDL receptor family receptors, relatively small reductio
99 receptor-related protein 1), a member of the LDL receptor family, acts as an endocytic receptor for B
100 nner that depends upon Lrp4, a member of the LDL receptor family, and muscle-specific kinase (MuSK),
101 hermore, we identified LRP1, a member of the LDL receptor family, as a new LeX carrier protein expres
103 for trafficking of megalin, a member of the LDL receptor family, from EE to the ERC by coupling it t
104 e interaction with the largest member of the LDL receptor family, low-density lipoprotein receptor-re
108 identified a novel low-density lipoprotein (LDL) receptor family member, termed LDL receptor class A
109 n antagonist of the low-density lipoprotein (LDL) receptor family, suggesting involvement of LDL rece
111 ubstantially raised LDL cholesterol, reduced LDL receptor function, xanthomas, and cardiovascular dis
112 antial reduction in low-density lipoprotein (LDL) receptor function, severely elevated LDL cholestero
113 taining mono- and biallelic mutations of the LDL receptor gene as models of familial hypercholesterol
114 or all members of the evolutionarily ancient LDL receptor gene family, is the major genetic modifier
115 ted prevalence of type 2 diabetes by APOB vs LDL receptor gene was 1.91% vs 1.33% (OR, 0.65 [95% CI,
116 Statins activate low-density lipoprotein (LDL) receptor gene expression, thus lowering plasma LDL
117 Members of the low-density lipoprotein (LDL) receptor gene family have a diverse set of biologic
118 c methods to evaluate the effect of diet and LDL receptor genotype on macrophage foam cell formation
120 or degradation via inducible degrader of the LDL receptor (IDOL) overexpression, using liver-targeted
121 diates posttranscriptional regulation of the LDL receptor in response to intracellular cholesterol le
122 lfate proteoglycans work in concert with the LDL receptor in the liver to facilitate binding and clea
123 f plasma Lp(a) levels, including the role of LDL receptors in the clearance of Lp(a), is poorly defin
125 9 (PCSK9) binds to low-density lipoprotein (LDL) receptors, increasing the degradation of LDL recept
127 e (LCAT) knock-out mice, particularly in the LDL receptor knock-out background, are hypersensitive to
129 native LDL, or ox-LDL and in hyperlipidemic LDL receptor knockout (LDLR(-/-)) mice that was effectiv
130 eloid alpha1AMPK knockout (MAKO) mice on the LDL receptor knockout (LDLRKO) background to investigate
131 8-deficient CD11c+ DCs into Western diet-fed LDL receptor knockout mice and found that the transplant
134 atherosclerotic lesion area was displayed in LDL receptor-KO mice transplanted with ERalpha(-/-) bone
135 mera containing the LDLa module of the human LDL receptor (LB2) demonstrated two key N-terminal regio
140 lesterolemia because of its ability bind the LDL receptor (LDLR) and enhance its degradation in endos
141 cholesterol (LDL-C) by interacting with the LDL receptor (LDLR) and is an attractive therapeutic tar
143 etary fatty acid composition on, lipoprotein-LDL receptor (LDLR) binding, and hepatocyte uptake, acco
146 importance of elevated circulating LDL, and LDL receptor (LDLR) expression in tumor cells, on the gr
147 ng of remnant lipoproteins to members of the LDL receptor (LDLR) family and cell-surface heparan sulf
148 at hnRNP K is specifically involved in human LDL receptor (LDLR) gene transcription in HepG2 cells.
151 hypercholesterolemia is typically caused by LDL receptor (LDLR) mutations that result in elevated le
152 ent of LDL, is known to bind to cell surface LDL receptor (LDLR) or cell surface-bound proteoglycans
158 sed by mutations in several genes, including LDL receptor (LDLR), apolipoprotein B (APOB), proprotein
159 d by variants in at least 3 different genes: LDL receptor (LDLR), apolipoprotein B-100, and proprotei
160 In humans and animals lacking functional LDL receptor (LDLR), LDL from plasma still readily trave
161 SK9 enhances the cellular degradation of the LDL receptor (LDLR), leading to increased plasma LDL cho
162 This multidomain protein interacts with the LDL receptor (LDLR), promoting receptor degradation.
163 cholesterol uptake receptors, including the LDL receptor (LDLR), the very LDLR, and the scavenger re
164 ible degrader of the LDL receptor) regulates LDL receptor (LDLR)-dependent cholesterol uptake, but it
172 rogenesis, we crossed mice deficient for the LDL receptor (Ldlr-/- mice) with mice that express low l
173 miR-33 inhibition in mice deficient for the LDL receptor (Ldlr-/- mice), with established atheroscle
175 icking, such as the low-density lipoprotein (LDL) receptor (LDLR) and the ATP-binding cassette A1 (AB
177 erosis by targeting low density lipoprotein (LDL) receptor (LDLR) degradation, this study investigate
178 9 (PCSK9) modulates low-density lipoprotein (LDL) receptor (LDLR) degradation, thus influencing serum
179 is interaction, the low-density lipoprotein (LDL) receptor (LDLR) has been proposed as a potential en
180 erexpression of the low density lipoprotein (LDL) receptor (LDLR) in HepG2 cells dramatically increas
182 se bone marrow into low-density lipoprotein (LDL) receptor (LDLr) knockout mice (SMS2(-/-)-->LDLr(-/-
183 ough PCSK9 controls low density lipoprotein (LDL) receptor (LDLR) levels post-transcriptionally, seve
185 equence analysis of low-density lipoprotein (LDL) receptor (LDLR) mRNA did not reveal any amino acid
186 degradation of the low-density lipoprotein (LDL) receptor (LDLR), and its deficiency in humans resul
187 d the expression of low-density lipoprotein (LDL) receptor (LDLr), sterol regulatory element-binding
190 ble degrader of the low-density lipoprotein [LDL] receptor [LDLR]) as a posttranscriptional regulator
192 proteases, binds to low-density lipoprotein (LDL) receptors, leading to their accelerated degradation
194 ess of monoclonal antibodies that extend the LDL-receptor lifecycle (and thus result in substantial l
197 alirocumab treatment suggests that increased LDL receptors may also play a role in the reduction of p
198 psin in the endoplasmic reticulum, deficient LDL receptor-mediated cholesterol uptake, and elevated l
199 possibility of a causal relationship between LDL receptor-mediated transmembrane cholesterol transpor
200 t and indisputably coexist, and both prevent LDL receptor-mediated uptake and promote macrophage scav
201 /kg/day) and AngII were co-infused into male LDL receptor -/- mice that were either AT2 +/y or -/y.
204 at prevent interaction of PCSK9 with hepatic LDL receptors (monoclonal antibodies, mimetic peptides),
209 Patients with 2 defective versus 2 negative LDL receptor mutations had mean LDL-C reductions of 23.5
210 gene (APOB) mutations, and receptor-negative LDL receptor mutations were considered more severe than
214 t vascular smooth muscle cells isolated from LDL receptor null (Ldlr(-/-)) mice, which have impaired
216 tein-restricted diet and 2) feeding C57BL/6J LDL receptor-null (LDLR(-/-)) dams a high-fat (Western)
218 xpansion were not significantly different in LDL receptor-null mice fed a saturated fat-enriched diet
219 potentially therapeutic protein can bind to LDL receptors on the BBB and be transcytosed into the CN
221 isulfide editing-dependent maturation of the LDL receptor or the reduction-dependent degradation of m
222 st to its previously reported effects on the LDL receptor, PCSK9 did not alter ENaC endocytosis or de
224 heparan sulfate proteoglycan (HSPG) and the LDL receptor, plus one docking receptor, SR-BI, signific
225 9 (PCSK9) binds to low-density lipoprotein (LDL) receptors, promoting their degradation and increasi
226 and activating a receptor complex containing LDL receptor protein 4 (Lrp4) and muscle-specific kinase
228 ssion lowered plasma PCSK9 levels, increased LDL receptor protein expression, and restored plasma cho
232 oblasts as a result of profound reduction in LDL-receptor protein, but not mRNA; heterologous express
233 uitin ligase IDOL (inducible degrader of the LDL receptor) regulates LDL receptor (LDLR)-dependent ch
234 se subtilisin/kexin type-9 (PCSK9, a hepatic LDL-receptor regulator), inflammation, and adipose tissu
239 l surface stimulates association of CRT with LDL receptor-related protein (LRP1) to signal focal adhe
242 sing a haploid genetic screen, we identified LDL receptor-related protein 1 (LRP1) as a host cell rec
247 rapid clearance of free Abeta40/42 from the LDL receptor-related protein 1 (LRP1) to the VLDL recept
248 epatic clearance of fVIII is mediated by the LDL receptor-related protein 1 (LRP1), a member of the L
249 ell biology techniques, we report that LRP1 (LDL receptor-related protein 1), a member of the LDL rec
251 hat tPA induces Tyr(4507) phosphorylation of LDL receptor-related protein 1, which in turn leads to t
252 nterstitial fibroblast proliferation through LDL receptor-related protein 1-mediated beta1 integrin a
255 identified a contribution of the annexin A6/LDL receptor-related protein 1/thrombospondin 1 (ANXA6/L
256 bular protein extracts that we identified as LDL receptor-related protein 2 (LRP2), also known as meg
257 he closely related WNT signaling coreceptors LDL receptor-related protein 5 (LRP5) and LRP6 had redun
259 y decreased expression of the Wnt coreceptor LDL receptor-related protein 6 (LRP6) in the mucosal tis
260 Loss-of-function mutations in Wnt coreceptor LDL receptor-related protein 6 (LRP6) underlie early-ons
261 f the frizzled (Fz) receptor, its coreceptor LDL receptor-related protein 6 (Lrp6), and the cytoplasm
265 ivation was determined by phosphorylation of LDL receptor-related protein 6, a coreceptor of Wnt liga
266 ular WNT activation by binding to the Kremen/LDL receptor-related protein receptors, was not seen wit
267 omposed of the receptor tyrosine kinase AXL, LDL receptor-related protein-1 (LRP-1), and RAN-binding
272 The endocytic and cell signaling receptor, LDL receptor-related protein-1 (LRP1), is reported to su
273 iption factor in SCs, unless counteracted by LDL receptor-related protein-1 (LRP1), which serves as a
279 tes express several Wnt receptors, including LDL receptor-related proteins 5 and 6, and Frizzled 1 to
280 ipoprotein E (ApoE) receptors, also known as LDL receptor-related proteins, have distinguished themse
282 nternalized through low-density lipoprotein (LDL) receptor-related protein-1 (LRP-1) to become enzyma
284 is a ligand for the Low Density Lipoprotein (LDL) Receptor-related Protein-1 (LRP1), a multifunctiona
286 structures of ligands in complex with tandem LDL receptor repeats or tandem CUB domains in other endo
288 h that contacted by the EGF(A) domain of the LDL receptor, suggesting a competitive inhibition mechan
293 ession of PCSK9, a secreted inhibitor of the LDL receptor, thereby limiting their beneficial effects.
294 targets, and that inhibition of ACL leads to LDL receptor upregulation, decreased LDL-C and attenuati
295 To this end, the low-density lipoprotein (LDL) receptor was targeted for degradation via inducible
296 Thus, by inducing hepatic degradation of the LDL receptor, we generated a T2D model of combined kidne
297 ely target cancer cells that overexpress the LDL receptor while showing minor adverse impact on norma
298 oth furin- and hepsin-cleaved PCSK9 bound to LDL receptor with only 2-fold reduced affinity compared
300 the role of AT(1a) receptors on leukocytes, LDL receptor(-/-)xAT(1a) receptor(+/+) or AT(1a) recepto
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